Pathology of Hypertension Flashcards
Hyaline Ateriolosclerosis
- Associated with what disease?
- Cause?
- Patient Profile?
- Appearance?
Disease Association:
• Benign Hypertension
Cause:
- Pressure pushes plasma proteins across injured endothelial cells
- Chronic Stress ^ increases matrix synthesis
Patient Profile:
• Hypertensive patients or Old people
Appearance:
• Thick Intima with very pink appearance from deposited proteins
Hyperplastic Arteriolosclerosis
- Associated with what disease?
- Cause?
- Appearance?
Disease Association:
• SEVERE (malignant) Hypertension
Cause:
- Increased strain causes Muscle cells to become thickened and duplicated
- FIBRINOID NECROSIS may also occur
Appearance:
- Onion Skinning appearance
- Amphoric and pink in the case of fibrinoid necrosis
Thrombosis
• cause of thrombosis in Vascular Disease?
Formation of a Blood Clot from Exposed ECM
• in this context Exposed ECM comes from ruptured plaque
Embolus
• cause?
Thrombus is mobilized and can move throughout vasculature
Atherolsclerosis
- Disease characterized by Intimal Lesions called artheromas
- these artheromas have a lipid core surrounded by a fibrous cap
Medial Calcific Sclerosis
- Common in people over 50 y/o where Calcium is seen in the intima
- Don’t freak out if you see this on a radiograph or mammogram as long as it follows a vessel its okay
What is the significance of: Turbulence, Dyslipidemia
• Two most common causes of endothelial injury leading to atherosclerosis
What is a Fatty Streak?
i
What is a Plaque?
i
What is Stenosis?
Occlusion of an artery caused by large atherosclerotic plaque
Aneurysm
Ballooning out of all 3 layers of a vessel due to weakening of the media
Dissection
i
T or F: Hypertension puts you at an increased risk for renal failure?
True, this risk is especially high in people with diabetes and hypertension
What are the cutoffs for hypertension?
140 mmHg systolic 90 mmHg diastolic
In what case might you place a patient with a blood pressure of lower than 140/90 on anti-hypertensive medication?
• High risk patients such as those with Diabetes may need treatment earlier than other people
T or F: in the case of hypertension preventative medicine has proven to be extremely effective.
True
What causes most cases of hypertension?
90% of cases are idopathic
What are some diseases that often have a secondary effect of hypertension?
• Renal Disease
• Renal Artery Narrowing
• Adrenal Disorders
Why is hypertension often a secondary result of many renal disorders?
- Macula Densa falsely Sense Low Blood Volume because of renal disease
- Increased Renin –> angiotensin I –> angiotensin II will lead to increased fluid volume and a heart that is beating harder
- Aldosterone may be secreted in too large amount in adrenal tumors etc. (pheochromocytoma)
How do you calculate Cardiac Output?
CO = Heart Rate x Stroke Volume
What is the standard response of the vascular wall to injury?
- Smooth Muscle Hyperplasia in INTIMA
- ECM is synthesized
- PERMANENT intimal thickening result
Atherosclerosis
- Cause
- Vessels involved
- Disease Type
Cause:
• LIPID Accumulation with Cellular Reaction
Vessels Involved:
• Large and Medium Arteries
Disease Type:
• Considered an INFLAMMATORY DISEASE
What are the most common arteries to see atherosclerosis in?
• Abdominal Aorta
• Coronary Arteries
• Cerebral
• Common Iliac
• Femoral Arteries
****What is this?
• Clinical Significance
Monckebergs
• Typically not clinically significant
**Monckebergs
- Cause
- Vessel type
- Appearance (radiology and H&E)
- Significance
Cause:
• Cacification of Vessel Media
Vessel:
• Muscular Arteries
Appearance:
- Dark purple calcium deposits in the media on H and E
- Follows the path of the vessel on Radiology
What patient population is Monckenbergs often seen in ?
• Ppl. 50 years and older commonly have Monckebergs
**Arteriolosclerosis
- Cause
- Vessel type
- Types
Cause:
• Reduced lumen size from thickening of vessel in response to high pressure
Vessel Type:
• Small Arteries
2 types:
• Hyaline
• Hyperplastic
What diseases are associated with arteriolosclerosis?
- Diabetes
- Hypertension
****What is this?
• key features?
Nephrosclerosis
• Pitting Scars on the surface that should be smooth
****What is this?
• Patients this is most commonly seen in?
Onion Skinning in Hyperplastic Arteriolosclerosis
• Most commonly seen in patients with malignant hypertension (>200mmHg systolic)
*****What is this?
• Patients this is most commonly seen in?
Hylaine arteriolosclerosis - intimal thickening from ECM expansion
• seen in Elderly and people with Benign Hypertension
*****What is this?
• Patients this is most commonly seen in?
Hyperplastic arteriolosclerosis that has caused Fibrinoid Necrosis of Small Renal Arteries
What organs are most commonly damaged in Hyperplastic Arteriolosclerosis?
Kidney Damage is common
What is an atheroma?
• Plaques of LIPID CORES covered by a FIBROUS CAP • Lesions found in the INTIMA
What is the difference in etiology of an acute occlusion vs. chronic occlusion of a large vessel lumen?
Chronic:
• Plaque slowly builds up by binding more and more LDL
Acute:
• Cap ruptures and underlying collagen etc. is exposed and leads to acute Myocardial Infarction
How can atheroclerotic plaques increase the probability of aneurysm?
• Lipids and Necrotic Tissue may weaken the intima and media causing a ballooning out (aneurysm) of the vessel
What are some of the constitutional risk factors for atherosclerosis?
Genetics:
- Mendelian Disorders (like FH)
- Polygenic traits (like Diabetes, HTN)
Age:
• 40-60 pts. may start to become symptomatic Gender: • Premenopausal Women are protected
What are some modifiable risk factors for atherosclerosis?
- Hyperlipidemia
- Hypertension
- Cigarettes
- Diabetes
- Inflammation (CRP and Hyperhomocysteinemia)
What is the first gross sign indicating where a clot might form?
• Fatty Streak
**What are the steps in formation an atherlosclerotic plaque?
- Chronic Endothelial Injury
- Endothelial Dysfunction attracts leukocytes, monocytes, and platelets
- Macrophages Recruit Smooth Muscle to the intima
- Macrophages and Smooth Muscle Cells eat LIPIDS
- Smooth muscle cells proliferate and deposit Collagen and ECM
What is secreted by T-cell in the atherlosclerotic plaque?
IFN-gamma
What does the fibrous plaque resemble underneath the microscope?
Granulation Tissue
What is the difference in stable and and unstable progression of atherloma?
Stable:
• Slow progression caused by accumulation of more and more lipid in the intima
***Leads to stable angina
Unstable:
• RAPID progression caused by platelet and fibrin deposition that expands and causes thrombus formation
How do you know a plaque is becoming unstable?
• 70% or more of the lumen is occluded - this characterizes and unstable plaque
What vessels are most commonly involved in Atherlosclerosis?
- INFRARENAL abdominal Aorta
- Coronary Arteries
- Popliteal Arteries
- Internal Carotid Arteries
- Circle of Willis
What are the ways in which Athlerosclerosis become clinically relevent?
• when does this happen?
40-60 y/o Disease Becomes Clinically Relevent 3 ways:
- Aneurysm (weakening of arterial wall)
- Thrombosis (ruptured plaque)
- Critical Stenosis (>70% vessel occlusion)
****What is this?
• Atherosclerotic Plaque
What are the 3 most common areas where plaques occur?
• Ostia of Existing Vessels
• Branch Points
• Posterior Wall of Abdominal Aorta
What roles does dyslipidemia play in formation of atherosclerotic plaque?
- Cholesterol impairs endothelial cell function causing an increase in free radicals that scavenge NO leading to less vasodilation
- LIPID ACCUMULATION in the intima becomes oxidized LDL and cholesterol clefts form - macrophages ingest this and become foam cells
****What do you see here?
- Cholesterol Clefts
- Foam Cells
What is the importance of cholesterol clefts in atherosclerosis?
• Cholesterol Clefts incite inflammation and Subsequent Release of IL-1
****What cell type is shown on the vessel surface seen here?
• Foam Cells
****What is this?
• Fibrous Cap of an atherosclerotic Plaque resembling granulation tissue
What typically makes of the cells of a plaque and the ECM?
Cells:
• Smooth Muscle
• Macrophages
• T-cells
ECM:
• Collagen
• Elastic Fibers
• Proteoglycans
• Cholesterol Clefts
****What is happening in this coronary artery?
- Thrombosis seen as red
- Recanalization of an old hemorrhage (seen as darker pink)
*****Would you consider this a stable or unstable plaque? why?
Stable because only thickening of the wall is seen and no hemorrhage or thrombosis is evident
*****Would you consider this plaque stable?
NO there is clear evidence of thrombus
*****What is this?
*Thrombus formation in descending interventricular coronary artery
****what process is seen here?
Thrombus from Ruptured Plaque
What are some of the clinical complications of atherosclerosis?
- Ischemia
- MI
- Stroke
- Aortic Aneurysms
- Peripheral Vascular Disease
What layers are involved in aneurysms?
All Three Layers
What is False Hematoma?
• Hematomas that communicate with the extravascular space
What are the characteristic symptoms of an aneurysm?
• Deep constant pain in abdomen accompanied by back pain
Why/How does atherlosclerosis put you at an increased risk of aneurysm?
- While atherlosclerosis is a disease of the intima but the plaque may compress and cause thinning of the media
- Weakening of the wall and loss of elasticity causes a predisposition for dilation and rupture
*****What is this patient about to get surgery for?
Abdominal Aneurysm
*****What disease causes a predisposition for the disease shown here?
Hypertension
• This is an ascending aortic dissection
******what disease causes a predisposition for the disease seen here?
Atherlosclerosis
• this is an abdominal aortic aneurysm
What genetic disorders put you at an increased risk of aneurysm?
- Collagen Defects
- Marfans or Type IV Ehlers-Danlos Syndrome
Syphilis is most likely to cause what type of aneurysm? • why does this happen?
Thoracic
• Happens as a result of inflammation around the VASO VASORUM
• Inflammatory cells are often plasma cells
****What pathological process is shown in this picture?
*Thoracic aneurysm
* Notice the Tree Bark Appearance
*****What pathological process is shown here?
• Who is at the greatest risk of experiencing this?
- Abdominal Aortic Aneurysm
- Male Smokers over 50 years old
Who is AAA typically seen in?
• complications?
Typically Male smokers over 50
Complications:
- Obstruction of Vessels Branching off of the aorta
- Embolism
- Impingement on Adjacent Structures
- Rupture
How does AAA feel?
* Feels like a pulsating tumor in the abdomen
****What processes is seen here?
• Dissection
****What processes is seen here?
• main risk factor
- Dissection of Ascending Aorta
- Risk Factor - Hypertension
What is the role of TGF-ß in the pathogenesis of Dissection?
• What is unique about aneurysms in people with TGF-ß dysregulation?
- TGF-ß regulates smooth muscle cell proliferation and matrix synthesis
- Mutations in TGF-ß receptors or Downsteam signaling pathways result in defective elastin and collagen synthesis
- ANEURYSMS in these people tend to RUPTURE even when SMALL
What is the pathophysiology that links Marfan Syndrome to Aneurysm?
- FIBRILLIN is abnormally synthesized
- TGF-ß is sequestered in aortic wall due to abnormal FIBRILLIN
- this results in DYSREGULATED SIGNALING that causes progressive loss of elastic tissue
Cystic Medial Degreneration
- what is it?
- what causes it?
What is it:
• Change in medial smooth muscle phenotype
Cause:
• ECM synthesis is defective due to ischemic changes of the outer media
How can Dissection in a patient cause Cardiac Tamponade?
• Dissection can travel Retrograde into the heart valves
****What is abnormal about the aortic wall shown here?
• Weak disorganized collagen can be seen which puts the patient at higher risk for Dissection or Aneurysm ***Disorganization at the top = major problem
